2. Signaling Pathways
  3. Cytoskeleton
  4. Cadherin

Cadherin

Cadherins are a family of calcium-dependent cell adhesion molecules and transmembrane glycoproteins that play a crucial role in maintaining tissue architecture and cellular communication. Key members of the cadherin family include E-cadherin (CDH1), N-cadherin (CDH2), and P-cadherin (CDH3), etc. Cadherins mediate cell-cell adhesion through homophilic interactions, forming adherens junctions that connect to the actin cytoskeleton via catenins, thus influencing cellular signaling pathways related to proliferation, differentiation, and migration[1].

cadherins are involved in various signaling pathways, such as the Wnt and Notch pathways, which are critical for development and tissue homeostasis. Cadherins often bind to β-catenin (CTNNB1) through the catenin-binding domain. The catenin-binding domain of cadherin is crucial in cadherin function and it plays an important role in maintaining epithelial integrity. Dysregulation of cadherin expression is associated with several diseases, particularly cancer, such as pancreatic cancer, melanoma, hepatocellular carcinoma, glioblastoma, breast and gastric cancers. The epigenetic silencing of cadherins through mechanisms like DNA methylation further exacerbates this issue in tumor progression. Understanding cadherins' roles in cellular dynamics provides insights into potential therapeutic targets for cancer and other diseases characterized by altered cell adhesion[1].

Cadherin Related Products (60):

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-181506
    TYMJ-01
    		Inhibitor
    TYMJ-01 is a fluorescent probe and eEF2K degrader. TYMJ-01 induces dose-dependent and specific degradation of eEF2K via the ubiquitin-proteasome pathway, with a DC50 of 82 nM. TYMJ-01 inhibits the proliferation, migration and invasion of triple-negative breast cancer cells. TYMJ-01 enables dynamic fluorescent imaging of eEF2K degradation in triple-negative breast cancer cells; it enhances the anti-tumor activity of Paclitaxel (HY-B0015). TYMJ-01 can be used for the research of triple-negative breast cancer.
    TYMJ-01
  • HY-175815
    Apoptosis inducer 44
    		Agonist
    Apoptosis inducer 44 is an apoptosis inducer. Apoptosis inducer 44 triggers apoptosis in MDA-MB-231 cells by increasing the levels of Bax and Cyt C, reducing Bcl-2, and initiating caspase-3 cleavage. Apoptosis inducer 44 suppresses the invasion and migration of MDA-MB-231 cells by down-regulating MMP-2 and MMP-9 expression and up-regulating E-cadherin protein levels. Apoptosis inducer 44 can be used for the study of breast cancer.
    Apoptosis inducer 44
  • HY-175257
    Theophylline-platinum(IV) prodrug-1
    		Inhibitor
    Theophylline-platinum(IV) prodrug-1 is a PARP-1 inhibitor. Theophylline-platinum(IV) prodrug-1 enhances DNA damage, ROS production, mitochondrial dysfunction, apoptosis and S-phase arrest, along with reducing invasion and metastasis in cells. Theophylline-platinum(IV) prodrug-1 exhibits superior antitumor activity in the xenograft SKOV3-BRCA1-KD tumor model. Theophylline-platinum(IV) prodrug-1 can be used for the study of ovarian cancer.
    Theophylline-platinum(IV) prodrug-1
  • HY-179623
    PI3Kα-IN-29
    		Inhibitor
    PI3Kα-IN-29 is a potent, orally active and selective PI3Kα with an IC50 of 2.5 nM. PI3Kα-IN-29 exhibits >400-fold selectivity over PI3Kβ/δ/γ/mTOR. PI3Kα-IN-29 selectively degrades the H1047R mutant p110α protein and inhibits PI3Kα kinase activity. PI3Kα-IN-29 suppresses PI3K/AKT/mTOR signaling, induces G1 arrest, and inhibits migration. PI3Kα-IN-29 inhibits tumor growth in a T47 mouse model. PI3Kα-IN-29 can be used for the research of breast cancer.
    PI3Kα-IN-29
  • HY-P11346
    N-Cadherin mimic peptide
    		Agonist
    N-Cadherin mimic peptide is a N-cadherin agonist. N-Cadherin mimic peptide promotes N-cadherin homodimerization via enhancing β-catenin signaling, inducing early chondrogenesis and cartilage matrix production in mesenchymal stem cells (MSCs). N-Cadherin mimic peptide is promising for research of MSC-based cartilage regeneration.
    N-Cadherin mimic peptide
  • HY-176861
    Hakin-1
    		Inhibitor
    Hakin-1 is a E3 Ubiquitin-Ligase Hakai inhibitor. Hakin-1 blocks Hakai-mediated global ubiquitination and specific ubiquitination of E-cadherin and inhibits epithelial-mesenchymal transition (EMT) progression. Hakan-1 inhibits tumor progression and cancer metastasis. Hakin-1 can be used for the study of carcinoma such as colorectal cancer.
    Hakin-1
  • HY-N16399
    Black tea extract
    Black tea extract is the extract of Black tea. Black tea extract prevents inorganic arsenic (iAs) induced ROS generation, inhibiting uncontrolled proliferation, epithelial to mesenchymal transition (EMT) and metastasis in HaCaT cells. Black tea extract has an anti-fibrotic activity. Black tea extract can be used for skin cancers research.
    Black tea extract
  • HY-181993
    JNK3-IN-11
    JNK3-IN-11 is a selective JNK3 inhibitor with an IC50 of 2.08 nM. JNK3-IN-11 binds to the JNK3 ATP-binding pocket, forming conserved hydrogen bonds with Met149 and a water-mediated hydrogen bond with Lys93. JNK3-IN-11 suppresses TGF-β1-induced c-Jun phosphorylation, reduces profibrotic markers COL1A1 and PAI-1, restores E-cadherin expression, and has protection against podocyte injure. JNK3-IN-11 can be used for the research of chronic kidney disease.
    JNK3-IN-11
  • HY-174247
    CPS-021
    CPS-021 is a selective PAK4 PROTAC degrader with a DC50 of 50 nM. CPS-021 has potent antimigratory and invasive activity and significantly suppresses the invasion and metastasis of tumor cells in A549-luc lung metastasis mice model. Pink: PAK4 ligand (HY-174822); Blue: CRBN ligase ligand (HY-10984); Black: linker
    CPS-021
  • HY-181717
    TKL002
    		Inhibitor
    TKL002 is a blood-brain barrier-permeable inhibitor of the CTH/H2S/NF-κB/EMT signaling axis. TKL002 induces G2/M phase cell cycle arrest and apoptosis in glioblastoma cells. TKL002 inhibits the migration and invasion of glioblastoma cells by upregulating E-cadherin and downregulating N-cadherin and vimentin. TKL002 is applicable to relevant research on glioblastoma.
    TKL002
  • HY-145269
    AL-GDa62
    		Inhibitor
    AL-GDa62 is a derivative of the CDH1/E-cadherin modulator SLEC-11 (HY-145268) and induces apoptosis in CDH1-/- cells. AL-GDa62 has an EC50 of 3.2 μM and 2 μM for isogenic mammary epithelial cells MCF10A-WT (wild type) and mutant MCF10A-CDH1-/-, respectively. AL-GDa62 specifically inhibits TCOF1, ARPC5, and UBC9, and suppresses SUMOylation at low micromolar concentrations.
    AL-GDa62
  • HY-N16719
    Picrasidine J
    		Activator
    Picrasidine J is a selective inhibitor targeting the KLK-10 protease and the ERK signaling pathway. Picrasidine J inhibits epithelial-mesenchymal transition (EMT) by upregulating E-Cadherin and ZO-1 and downregulating β-catenin and Snail, while simultaneously reducing KLK-10 expression and inhibiting ERK phosphorylation, thereby exhibiting significant anti-migratory and anti-invasive activity. Picrasidine J can inhibit the metastasis of head and neck squamous cell carcinoma (HNSCC) and is primarily used in anti-metastasis research for head and neck tumors.
    Picrasidine J
  • HY-172551
    anti-TNBC agent-9
    		Modulator
    anti-TNBC agent-9 (Compound 3as) is an anti-cancer agent for triple-negative breast cancer (TNBC). anti-TNBC agent-9 exhibits significant inhibitory activity against MDA-MB-453 cells with an IC50 value of 8.5 μM. anti-TNBC agent-9 inhibits tumor cell migration by upregulating E-cadherin and downregulating N-cadherin, matrix metalloproteinase 2 (MMP2), and MMP9. anti-TNBC agent-9 induces apoptosis by increasing the expression of the pro-apoptotic protein BAX and decreasing the expression of the anti-apoptotic protein BCL-2, thereby inhibiting tumor cell proliferation.
    anti-TNBC agent-9
  • HY-181556
    JNK3-IN-10
    		Activator
    JNK3-IN-10 is a blood-brain barrier-impermeable JNK3 inhibitor (IC50=0.257 nM) with over 400-fold selectivity over JNK1. JNK3-IN-10 blocks the JNK3-mediated signaling pathway downstream of TGF-β1, inhibits TGF-β1-induced phosphorylation of c-Jun, reduces the expression of pro-fibrotic markers, and restores the expression of the epithelial protein E-cadherin. JNK3-IN-10 exhibits low cytotoxicity, anti-fibrotic, cytoprotective and renoprotective effects, and alleviates albuminuria, glomerulosclerosis and podocyte foot process fusion. JNK3-IN-10 can be used for the research of chronic kidney disease, glomerulosclerosis and adriamycin-induced nephropathy.
    JNK3-IN-10
  • HY-P11154
    HAV peptide
    		Modulator
    HAV peptide (Ac-SHAVSS-NH2) is a peptide containing His-Ala-Val. HAV peptide affects the E-cadherin signaling pathway. HAV peptide regulates intercellular junctions.
    HAV peptide
  • HY-175291
    Cystatin B agonist 1
    		Activator
    Cystatin B agonist 1 is an orally active MMP-2/9 inhibitor. Cystatin B agonist 1 exhibits inhibitory effects with IC50 values of 3.95 and 3.43 μM against U87 and T98G cells, respectively. Cystatin B agonist 1 induces the cell-cycle arrest at S phase, inhibits angiogenesis, and suppresses migration and invasion of MG cells. Cystatin B agonist 1 inhibits tumor growth in U87 MG xenograft model. Cystatin B agonist 1 can be used for the study of malignant glioma (MG).
    Cystatin B agonist 1
  • HY-177374
    Ecad saRNA
    		Activator
    Ecad saRNA is a small activating RNA (saRNA) targeting the E-cadherin genes. Ecad saRNA induce expression of the E-cadherin genes, and targets the E-cadherin promoters at ?215 relative to gene's transcription start site.
    Ecad saRNA
  • HY-160187A
    (Rac)-AAA
    		Activator 99.02%
    (Rac)-AAA is a regulator and inhibitor targeting GPR75. By blocking the 20-HETE-induced downregulation of GPR75 expression, (Rac)-AAA effectively inhibits the activation of key downstream signaling pathways including EGFR, AKT, NF-κB and FAK. (Rac)-AAA reverses 20-HETE-mediated epithelial-mesenchymal transition, which is specifically characterized by downregulating vimentin (vimentin), upregulating E-Cadherin, as well as reducing MMP-2 activity and cancer cell migration ability. (Rac)-AAA also abolishes the 20-HETE-induced upregulation of HIC-5 expression and anchorage-independent growth, and modulates the subcellular localization of PKC-α and phosphorylated AKT. (Rac)-AAA is investigated in androgen-independent prostate cancer (castration-resistant prostate cancer).
    (Rac)-AAA
  • HY-177477
    2,5-Epidithia-3,6-dioxopiperazine
    		Inhibitor
    2,5-Epidithia-3,6-dioxopiperazine (Formula 15) is a derivative of Epidithiodioxopiperazine (ETP). 2,5-Epidithia-3,6-dioxopiperazine improves intracellular penetration and restores the activity of 2-Cys-Prx (especially Peroxiredoxin II (PrxII)) of form simulation in cells. 2,5-Epidithia-3,6-dioxopiperazine inhibits PDGF-induced proliferation and migration in vascular smooth muscle cells while promoting these actions in endothelial cells with VEGF induction. 2,5-Epidithia-3,6-dioxopiperazine effectively inhibits the proliferation and migration and lung metastasis of melanoma cells. 2,5-Epidithia-3,6-dioxopiperazine can be used for vascular diseases such as hypertension, angina pectoris and myocardial infarction research.
    2,5-Epidithia-3,6-dioxopiperazine
  • HY-P991341
    FF-21101
    		Inhibitor
    FF-21101 is a human IgG1 monoclonal antibody (mAb) targeting CDH3/P-cadherin. Recommend Isotype Controls: Human IgG1 kappa, Isotype Control (HY-P99001).
    FF-21101